Pulm Flashcards
What’s the earliest a pre-mature baby can survive?
25-26 weeks. By this point, the alveoli have developed so gas exchange (breathing) is possible.
What does atalectasis mean?
Collapsing of the alveoli
What is aspiration?
When food or vomit gets into the airways
What’s more anterior- the trachea or the esophagus?
The trachea
What are causes (3) of hypercapnia?
Hypercapnia= high CO2 in the blood. Causes:
- Fever (increased metabolic activity)
- Hypoventilation (blowing off less CO2)
- Dead space (ventilation w/o perfusion. There is a blood flow problem, so CO2 is remaining in the blood rather than getting pushed into alveoli)
Does shunting (perfusion w/o ventilation) lead to hypercapnia (inc CO2)? Explain.
No. You have a ventilation problem but blood will shunt to the alveoli that are working and shunted away from the alveoli that are not working/ not ventilating/ not capable of gas exchange. So CO2 will not build up. *you will get inc CO2 in the case of dead space where you have a blood flow problem that prevents the CO2 in blood from getting pushed up into the alveoli
What is dyspnea?
Shortness of breath (SOB)
When does lung development begin in embryo?
Week 4
What structure do the lungs develop from in embryo?
The lung bud (“respiratory diverticulum”)= outgrowth of the GI tract (specifically the foregut, or future esophagus)
Explain the main events in each stage of lung development: (1) embryonic (weeks 4-7), (2) pseudoglandular (weeks 5-17), (3) canalicular (weeks 16-25), (4) saccular (week 26-birth), and (5) alveolar (week 36-8 years).
(1) embryonic (weeks 4-7): lung bud branches down to tertiary bronchi
(2) pseudoglandular (weeks 5-17): there’s branching all the way down to terminal bronchioles (lungs resemble a gland)
(3) canalicular (weeks 16-25): terminal bronchioles further branch into respiratory bronchioles and alveoli w/ lots of capillaries. Pneumocytes develop at 20 weeks (type II pneumocytes make surfactant).
(4) saccular (week 26-birth): alveoli further develop and form sacs (seperated by septae)
(5) alveolar (week 36-8 years): “alverolarization” (alveoli get subdivided by septa walls so that they are smaller but there’s triple the amount—> inc surface area)
What is oligohydramnios? Why is this a problem for lung development?
Decreased amniotic fluid (from fetal kidney problem—> dec urine= dec amniotic fluid production) (part of Potter sequence). The baby in embryo needs to swallow amniotic fluid to expand their developing lungs. Amniotic fluid fills baby’s lungs and stimulates further development of the lungs. W/o enough amniotic fluid, the baby is born with PULMONARY HYPOPLASIA= underdeveloped lungs.
What is pulmonary hypoplasia?
Underdeveloped lungs. Associated with congenital diaphragmatic hernia (pleuroperitoneal membrane not formed properly—> hole in diaphragm—> abdominal organs herniate into chest and prevent proper lung development) and bilateral renal agenesis (fetal kidney problem—> lack of urine= lack of amniotic fluid—> lungs aren’t stimulated to develop fully)
What are bronchogenic cysts?
Abnormal budding of the foregut and dilation of terminal/ large bronchi. Cysts are fluid filled, lined by respiratory epithelium, contain cartilage
What is bronchopulnoary dysplasia?
Lung disease that affects premature babies. Caused by damage from mechanical ventilation (O2 toxicity, lung trauma)—> alveolarization (alveoli subdividing so you have more, smaller alveoli= inc SA) doesn’t progress normally—> respiratory problems during infancy (but often improves in childhood as lungs continue to develop).
What are club cells?
Non-ciliated cells in bronchioles (beginning of respiratory zone). Secrete a component of surfactant and do detoxification.
Describe type I and type II pneumocytes (alveoli cells).
TYPE I: makes up 97% of your alveolar cells. Line the alveoli. Squamous and thin for optimal gas exchange.
TYPE II: secrete surfactant to dec surface tension and prevent alveolar collapse. Cuboidal. Also can proliferate into other cells during lung damage to help heal the lungs.
What ingredients is surfactant made of?
Lecithins. The most important one is DPPC (dipalmitoylphosphatidylocholine)
During what week of development does surfactant start getting made?
Week 26
What is neonatal respiratory distress syndrome (NRDS)? What are 3 risk factors?
Surfactant deficiency (breathing disorder from immature lungs). Risk factors: premature baby, maternal diabetes (insulin dec surfactant production) C-section delivery (cortisol inc surfactant production and C-sections= less stressful delivery= less cortisol= less surfactant production).
What test can we do to screen for fetal lung maturity?
Lecithin-sphingomyelin. Lecithin (what surfactant is made of) should shoot up late in pregnancy when the baby lungs mature. A ratio of >2 is healthy. If <1.5 that’s predictive of NRDS (neonatal respiratory distress syndrome= surfactant deficiency= baby born with immature lungs and will need help breathing for a while)
Starting with the trachea, name all the respiratory tract anatomical structures in order.
Trachea—> primary bronchus—> secondary bronchus—> tertiary bronchus—> bronchioles—> terminal bronchioles (end of conducting zone)—> (start of respiratory zone) respiratory bronchioles—> alveoli
What is the general purpose of the conducting zone? Respiratory zone?
Conducting zone: warms, humidifies, and filters air. Respiratory zone: does gas exchange.
What kind of cells secrete mucous as a way of protecting against infection?
Goblet cells in the bronchi.
How many lobes make up the right lung? Left lung?
Right lung: 3 (upper lobe, middle lobe, lower lobe)
Left lung: 2 (upper lobe and lower lobe) heart on this side!
What is the carina?
The point where the trachea branches/ bifrucates into the right and left bronchus
If you aspirate a foreign body, like a peanut, where in the lungs is it most likely to end up—if you were standing up? Laying down?
Most likely to get into the RIGHT lung bc it doesn’t have to take as sharp of a turn going from trachea into right bronchus (as compared to trachea to left bronchus). It will always fall to the lowest point by gravity so…
Standing up—> goes to right lower lobe (inferior part)
Laying down—> goes to right upper or lower lobe (posterior part)
What accessory muscles (muscles other than the diaphragm) are used to breathe during exercise or respiratory distress?
Inspiration—> muscles from the neck (scalenes, SCM)
Expiration—> muscles from the abdomen (rectus muscle, internal and external obliques, transverse abdominis, internal intercostals)
What structures perforate the diaphragm at T8, T10, and T12?
T8: IVC, right phrenic nerve
T10: esophagus, vagus nerve/ CN 10
T12: aorta (red), thoracic duct (white), and azygos vein (blue) (“at T-1-2 it’s red, white, and blue”)
“I (IVC) ate (T8) ten (T10) eggs (esophagus) at (aorta) noon (T12)”
What nerve innervates the diaphragm and what spinal levels does it stem from?
Phrenic nerve. C3, C4, C5 keeps the diaphragm alive!
What is inspiratory reserve volume (IRV)?
The extra volume of air you can breathe in beyond normal inspiration
What is tidal volume (TV, or Vt)?
The volume of air you normally breathe in/ out (with each quiet inspiration, typically 500mL)
What is expiratory reserve volume (ERV)?
Extra volume of air you can breathe out beyond normal expiration
What is residual volume (RV)? Can you use spirometry to determine it?
The volume of air that stays in your lungs after you breathe out (no matter how hard you blow out). NO! Spirometry can only measure what you CAN blow out into the machine.
What is inspiratory capacity?
The full capacity you can breathe in
IRV + TV (inspiratory reserve vol, or the extra vol you can breathe in + tidal volume, or the normal vol you breathe)
What is functional residual capacity (FRC)?
The volume of air in the lungs after you breathe out
RV + ERV (residual vol, or the vol of air that stays behind in the lungs no matter how hard you blow out + expiratory reserve volume, or the extra vol of air you could breathe out if you blew out harder than normal expiration)
What is vital capacity (VC) also known as forced vital capacity (FVC)?
Max volume of air you can forcibly breathe out after max inspiration
TV + IRV + ERV (tidal volume, or the vol of air you normally breathe + inspiratory reserve volume, or the extra vol of air you can breathe in + expiratory reserve vol, or the extra vol of air you can breathe out)
What is total lung capacity (TLC)?
Vol of air in lungs after max inspiration (the total amount of air that can be in your lungs)
IRV + TV + ERV + RV (sum of all 4 lung volumes)
What is physiological dead space? What’s the difference between anatomic dead space and alveolar (functional) dead space?
In general dead space= air that doesn’t participate in gas exchange.
Physiological dead space= anatomic dead space + alveolar (functional) dead space.
Anatomic dead space= conducting airways (nasal cavity to terminal bronchus) that doesn’t do gas exchange.
Alveolar (functional) dead space= air stuck in alveoli not doing gas exchange bc the alveoli aren’t working well.
Thinking about elastic recoil, what is the tendency of lungs? The chest wall?
Tendency of lungs is to collapse inward. Tendency of chest wall is to spring outward. These forces balance each other.
Describe the structure of adult Hemoglobin (Hb A).
Hb= heme + globin. Heme is made up of iron (Fe) + protoporphyrin. Globin is made up of 2 alpha chains and 2 beta chains.
What is methemoglobin? How do you get this problematic form of Hb? What is the clinical presentation? What is the treatment?
Hemoglobin with Fe3+ (oxidized) instead of Fe2+. Why is this bad? Fe3+ doesn’t bind to oxygen well and you need Hb to bind to oxygen to go deliver it to tissues! And when Fe3+ does bind oxygen, it makes it to where the oxygen cannot be released to tissues.
Get this from nitrites and Benzocaine (med to numb throat before endoscopy).
Present with cyanosis and chocolate colored blood (dark in color bc not getting oxygen).
Treat with methylene blue (and vitamin C).
What is carboxygemoglobin?
Hemoglobin bound to CO (carbon monoxide) instead of oxygen. Bad bc you need Hb to bind oxygen to go deliver it to tissues!
How can you get CO (carbon monoxide) poisoning (leading to carboxyhemoglobin= Hb bound to CO rather than oxygen)?
Forest, car exhaust, gas heaters
How can you get cyanide poisoning?
Inhalation injury (like from fires)
What things shift the oxygen-Hb curve to the right? Explain.
Right shift= inc oxygen unloading to tissues. Remember in terms of exercise: Exercise, inc temp, inc CO2 (from inc tissue metabolism in exercise), dec pH/ inc H+ (think of lactic acid buildup in exercise from metabolism). Also high altitude will shift right (need more delivery of oxygen to tissues since you’re oxygen deprived) and inc 2,3-BPG will shift right (this molecule in RBCs promotes Hb to release oxygen).
What is the Bohr effect?
When you have inc CO2, the Hb-oxygen curve will shift right= more unloading of oxygen to tissues.
**Exercise, inc temp, inc CO2 (from inc tissue metabolism in exercise), dec pH/ inc H+ (think of lactic acid buildup in exercise from metabolism).
In hypoxia, do you have vasodilation or vasoconstriction going on in (1) systemic circulation and (2) pulmonary circulation? Explain.
Systemically you have vasodilation (dec BP, inc blood flow) to inc blood flow and therefore inc the oxygen getting to tissues to compensate for the low oxygen state you are in.
In pulmonary circulation you have the opposite—vasoconstriction (inc BP, dec blood flow). Why? The lungs will shunt blood away from poorly ventilated areas
What’s perfusion-limited? Diffusion-limited?
Perfusion-limited means gas equilibrates/ diffuses before the blood gets there (blood is the “slow guy” limiting the rate of gas exchange).
Diffusion-limited means blood gets there before the gas can equilibrate/ diffuse (the gas itself is the “slow guy” limiting the rate of gas exchange).
What is the equation that involves pulmonary vascular resistance (PVR) that can tell you about all the causes of pulmonary HTN? (Hint: starts with Ppa, or pressure of pulmonary arteries, equals…)
Ppa= CO * PVR + Pla
(Pressure of pulmonary arteries = cardiac output * pulm vascular resistance + pressure in LA)
*if Ppa is high that means pulmonary HTN, and can be due to any of the other variables being high.
How do you calculate A-a gradient? What does it mean conceptually? What is a normal A-a gradient value?
A-a= P(A)O2 - P(a)O2
(Oxygen in Alveoli - oxygen in arteriole/ capillary)
Tells you about how well oxygen is diffusing across from the alveoli to the capillary in gas exchange. Normal= 10-15mmHg (for example, oxygen in Alveoli= 100. Oxygen in capillary= 90 bc there is a little blood that normally flows past w/o getting oxygenated. A-a= 100-90= 10= normal. If A-a were high (>15) you’d know air is having a hard time diffusing across the alveoli and interstitium to get to capillary—> hypoxemia (low oxygen in blood))
Why is TB most often seen in the apex of the lungs (vs. the base of the lungs)?
The apex of the lungs has the highest V/Q ratio. That means the most oxygen is available at the apex and TB likes that.
Where in the lungs (apex, middle, or base) is ventilation (V) highest? Perfusion (Q)? V/Q ratio?
Highest V and Q at the base of the lungs (think of it as more oxygen and blood will go there due to gravity). Highest V/Q ratio at apex of lungs (due to small V/ smaller Q= bigger ratio) so more oxygen is available for gas exchange at the top of the lungs (*this is why organisms like TB thrive at the apex- they like oxygen).
What is a shunt? Dead space?
Shunt= perfusion w/o ventilation (complete blockage of ventilation through alveoli). V/Q= 0/#= 0.
Dead space= ventilation w/o perfusion (blood flow blockage). V/Q= #/0= infinity.
What 2 criteria are needed to rule out obstructive lung dz?
FEV1/FEV ratio > 0.7 AND FVC is normal (not reduced)
*for the purposes of board exams, if FEV1/FEV is <0.8 it’s obstructive. If >0.8 it’s restrictive.
In very general terms, what is the difference between obstructive and restrictive lung disease?
Restrictive= problem getting air in/ inhaling (alveoli problem, like in fibrosis) “too small of a cup” Obstructive= problem getting air out/ exhaling (airway problem, like in COPD, chronic bronchitis, asthma) “too narrow of a straw to slurp up that milkshake”
Do you see increased, normal, or decreased RV, FRC, and TLC in obstructive lung dz? How about restrictive lung dz?
(RV= vol left in lungs no matter how hard you blow out, FRC= vol air in lungs after breathing out normal, TLC= vol of air in lungs after max inspiration, or sum of all lung volumes)
Obstructive (problem getting air out)—> increased RV, FRC, TLC (air trapped)
Restrictive (problem getting air in)—> decreased RV, FRC, TLC (less air left behind in lungs bc you breathe in less air to begin with)
What’s a normal FEV1/FEV ratio?
0.8 (80%)
Though some textbooks may say 0.7
What is FEV1 and FEV (conceptually)? What happens to those values (increase, stay same, or decrease) and to the FEV1/FEV ratio in restrictive lung dz? Obstructive lung dz?
FEV1 (fraction expired volume in 1 sec.)= max air you can blow out in 1 sec.
This is decreased in restrictive (problem getting air in= less air in= less air out) but decreased more in obstructive (problem getting air out, and they have the hardest time getting air out initially).
FEV (fraction expired volume)= max air you can blow out after max inspiration.
This is decreased in restrictive (problem getting air in= less air in= less air out) and decreased equally in obstructive (problem getting air out).
FEV1/FEV is normal or increased in restrictive (problem getting air in and dec FEV1/ dec FEV= normal.
FEV1/FEV is decreased in obstructive (problem getting air out and really dec FEV1/ dec FEV= dec ratio) (**But, it is possible to have inc ratio in obstructive disease if FEV is even lower than FEV1…this is why to rule out obstructive disease you must have both a big ratio of FEV1/FEV> 0.8 AND a normal, not lowered, FVC—learned in first year, but not important for board exams)
What is the atopic triad?
Allergic rhinitis, asthma, eczema
A kid has allergic rhinitis and eczema. What 3rd condition is the kid likely to have?
Asthma. Atopic triad= allergic rhinitis + asthma + eczema (3 allergy conditions that often go together)
What is rhinitis and what’s the most common cause of it?
Common cold. Rhinovirus.
Kid with nasal polyp. What should you test the kid for?
Cystic fibrosis (note: nasal polyps form from repeated bouts of rhinitis= inflammation of the nasal mucosa, or the common cold)
What are the 2 causes of nasal polyps (in Pathoma)?
Cystic fibrosis and aspirin- intolerant asthma (note: nasal polyps form from repeated bouts of rhinitis= inflammation of the nasal mucosa, or the common cold)
What is the triad seen in aspirin-induced asthma?
(1) asthma (2) aspirin-induced bronchospasms (3) nasal polyps (seen in 10% of asthmatic adults)
* think of it like asthmatics that are allergic to aspirin/ don’t tolerate it well (the nasal polyps form from repeated bouts of rhinitis= inflammation of the nasal mucosa, or the common cold)
Adolescent male with non-stop nosebleeds. What are you thinking of?
Angiofibroma (benign nasal tumor of the blood vessel)
African kid or Chinese adult with history of EBV. Presents with swollen cervical lymph nodes and mass in the nasopharynx. Biopsy reveals pleomorphic keratin-positive cells. What is the most likely diagnosis?
Nasopharyngeal carcinoma (note: keratin-positive means Epithelial cells and carcinoma= cancer arising from epithelial cells)
What’s the most common cause of acute epiglottitis?
H. Influenza type B (vaccinated kids can get it too bc vaccines aren’t perfect, but usually will see it in an un-vaccinated child)
What does carcinoma mean?
Malignant cancer arising from Epithelial cells
Kid comes in with fever, sore throat, drooling, muffled “hot potato” voice, and inspiratory Stridor. What’s the most likely diagnosis?
Acute epiglottitis (from H. Flu type B) (Symptoms are from larynx inflammation and airway obstruction)
Kid with barking cough and inspiratory stridor. What is it?
Laryngotracheobronchitis, or Croup. Most likely from parainfluenza virus. (Note: inspiratory stridor is due to inflammation blocking the large airways)
A singer presents with hoarseness to the voice and a nodule on her true vocal chord. What is the most likely diagnosis?
Vocal chord nodule, or “signer’s nodule” (due to overuse of vocal chords, made of connective tissue, resolves with resting of the voice)
Kid presents with hoarseness and benign growth (finger-like projection) on the vocal chord. What cell type are you most likely to see on histology?
Koilocytes. This is a laryngeal papilloma due to HPV 6 and 11.
Kid presents with benign growth of the vocal chord. What virus is associated with this?
This is a laryngeal papilloma. Answer= HPV 6 and 11.
What is the difference between laryngeal papilloma and laryngeal carcinoma? What are the risk factors/ what brings it on?
Laryngeal papilloma= benign tumor, projection off of the vocal chord. Associated with HPV 6 and 11.
Laryngeal carcinoma= squamous cell carcinoma arising from the epithelial lining of the vocal chord. Risk factors= alcohol and tobacco (inc risk for pretty much any throat/ mouth CA due to the chronic inflammation they cause).
What’s the difference between the pneumonia types: lobar pneumonia, bronchopneumonia, and interstitial/ atypical pneumonia?
LOBAR PNEUMONIA- consolidation (fluid) of an entire lobe
BRONCHOPNEUMONIA- consolidation around bronchioles (small airways) (patchy)
INTERSTITIAL (ATYPICAL) PNEUMONIA- no consolidation but inflammation is in the interstitium (you’d see increased lung markings on X-ray)
What’s the most common cause of community-acquired pneumonia? What’s the most common cause of secondary pneumonia (you get a viral infection and then pneumonia)?
Most common cause of pneumonia- STREP PNEUMO.!
Most common cause of secondary pneumonia- still STREP PNEUMO. 2nd most common secondary pneumonia is STAPH AUREUS.
What are the 4 gross phases of lobar pneumonia?
(1) congestion (inflammation of vessels and edema)
(2) red hepatization (lung takes on a solid liver-like look rather than its normal spongy look—this is due to exudate, inflammatory cells, and blood from the leaky inc vascular permeability vessels)
(3) gray hepatization (cells die)
(4) resolution (the lung heals by type II pneumocytes acting as stem cells to regenerate the alveolar lining)
Patchy consolidation around bronchioles. What kind of pneumonia are we talking?
Bronchopneumonia
What category of pneumonia is characterized by diffuse interstitial infiltrates?
Interstitial (atypical) pneumonia
Fever. Chills. Productive cough with yellow-green sputum (pus) or rusty (blood) sputum. Tachypnea (rapid, shallow breathing) with pleuritic chest pain. Dullness to percussion. Elevated WBC count. What are you thinking (general diagnosis)? Explain these symptoms/ findings.
Pneumonia (infection of the lung parenchyma= functional part of the lungs). Occurs when normal defenses are impaired (impaired cough reflex, damage to mucociliary escalator, mucus plugging). The infection causes cough bc that’s your body’s reflex to get the bacteria/ organism causing it out of there. You get pleuritic chest pain bc bradykinin and PG E2 are inflammatory mediators released and you are stretching out the lungs when you breathe in. Dullness to percussion indicates fluid/ consolidation.
How do we diagnosis pneumonia besides history and physical exam? (in other words, what tests do we get)
Chest X-ray, sputum gram stain and culture, and blood cultures (organisms are often in the blood)
Why does diabetes increase one’s risk for developing Klebsiella pneumoniae and all infections in general?
Diabetes= inc sugar in blood. Bacteria thrive on that sugar.
Alcoholic in a nursing home has a nasty cough going on and is coughing up thick, currant jelly sputum. What are you thinking?
Klebsiella pneumoniae.
Why are alcoholics at increased risk for Klebsiella pneumoniae?
You get it from aspirating enteric (GI) flora. For example, you vomit and breathe that up. Alcoholics vomit more and are more likely to choke on their own vomit while intoxicated.
Why are you at increased risk for getting a bacteria pneumonia (like strep pneumo or staph a.) following the flu (or right after any kind of viral infection)?
The virus knocks out the mucociliary escalator (part of your defense for pushing bad stuff out of the body)—> you become more susceptible to bacteria without this defense.
What 3 types of pneumonia are more often seen in COPD patients (leads to exacerbation of COPD)?
H. Flu, moraxella, and legionella
Pneumonia + diarrhea. What are you thinking?
Legionella! (Other hints: community-acquired pneumonia, smokers, water heaters, silver staining, not seen on normal gram stain)
What type of pneumonia is common among Cystic Fibrosis patients?
Pseudomonas aeruginosa
What’s the most common type of atypical/ interstitial pneumonia?
Mycoplasma penumoniae
After getting Mycoplasma pneumoniae, a patient develops hemolytic anemia and erythema multiforme. Explain.
Mycoplasma pneumoniae—> production of IgM antibodies to fight it off—> these IgM antibodies can attack RBCs (complication/ autoimmune process). Also note that these IgM antibodies do “cold agglutination.”
Erythema multiforme= target lesions (don’t know why they can get these, but also think of it as part of the autoimmune sequelae)
Why is Mycoplasma pneumoniae not visible on gram stain?
It lacks a cell wall.
What is the second most common cause of atypical/ interstitial pneumonia in young adults (after Mycoplasma pneumoniae)?
Chlamydia pneumoniae
What’s the most common atypical/ interstitial pneumonia in infants?
RSV (respiratory syncytial virus)
A post-transplant patient got an atypical/ interstitial pneumonia. What’s the most likely cause?
CMV (cytomegalovirus)
Can influenza virus cause pneumonia?
Yep. It can directly cause an atypical/ interstitial pneumonia. It can also indirectly cause a secondary pneumonia because the viral will knock out the cilia, making you more susceptible to then getting a bacterial pneumonia like strep pneumo or staph aureus or H. Flu.
A farmer just delivered a baby cow yesterday. Now he comes to you with a throbbing headache, high fever, cough, no rash. What are you thinking?
Coxiella burnetii. (Atypical/ interstitial pneumonia)
*you get this bacteria by contact with spores on cattle ticks or with cattle placentas
A right lower lobe abscess is a classic finding in what lung pathology?
Aspiration pneumonia (examples: Bacteroides, Fusobacterium, Peptococcus, Klebsiella). Why? Because aspiration= breathe your vomit or foot/ foreign object. Aspired things are more likely to go down the right bronchus (less of an angle to turn down) and settle in the right lobe of the lung, where they cause lung abscess (necrosis to an area of the lung).
If you are exposed to TB you’re immune system either deals with it, no problem OR you get a primary infection. Is the primary infection symptomatic? How about a secondary infection? Name the classic symptoms.
Primary infection of TB is NOT symptomatic (if you are infected with TB and don’t have a TB test done to check for exposure, you wouldn’t even know…goes latent…then if immune system weakens like from AIDS or stress, you get a nasty secondary infection).
Secondary infections ARE symptomatic: fever, night sweats, hemoptysis (coughing up blood), weight loss
TB affects what part of the lung—in primary infection? In secondary infection?
Primary infection—> lower lobe
Secondary infection—> upper lobe
A biopsy for TB would reveal what?
Caseating granulomas
What would you see upon staining of TB?
Acid-fast bacilli
What is the bone infection that TB can cause if it progresses to the point that it gets into the bones (usually the lumbar vertebrae)?
Pott disease.
*other systemic manifestations of TB: military TB (scatters all over), meningitis (gets into meningitis—> inflam.), inflammation of the cervical lymph nodes, sterile Pyuria of the kidneys
In a primary TB infection, there is formation of Ghon complexes. Explain.
The TB causes caseating necrosis in the lower lobe of the lung and hilarity lymphadenopathy. These hilar lymph nodes undergo fibrosis and calcification—> Ghon complex formation. Walls off the infection.
What are the 2 TB tests called?
PPD skin test (type 4 hypersensitivity) and IGRA blood test
What is COPD?
Chronic bronchitis + emphysema
In general, what is an obstructive lung disease? In general, what is a restrictive lung disease?
Obstructive= Problem getting air out/ exhaling Restrictive= Problem getting air in/ inhaling
What happens to FEV1, FVC, and FEV1:FVC ratio in obstructive pulmonary disease? Restrictive pulmonary disease? Explain why.
Obstructive= problem getting air out. FEV (max air you can breathe out) is decreased and FEV1 (max air you can breathe out in the first second) is decreased even more bc most air gets out in the first second of healthy people, but these patients have a problem getting air out and they breathe out air SLOWLY to protect airways from collapse, so especially will show a problem in that first second. This means FEV1:FVC ratio is decreased. RESTRICTIVE= problem getting air in. Both FEV and FEV1 are decreased because less air in= less air out, but FEV1 isn’t decreased as much because since the problem isn’t due to getting air out, they won’t have a problem blowing air out fast. So, FEV1:FVC ratio is increased.
In asthma, is TLC normal, increased, or decreased?
Asthma= obstructive= problem getting air out. TLC (total lung capacity) is the total amount of air that is in the lungs. So, TLC will be INCREASED due to air trapping (you can’t get as much air out).
What is the defining criteria for having chronic bronchitis?
Chronic productive cough lasting at least 3 months over a minimum of 2 years
What does a “caseating granuloma” mean?
Caseating= “cheesy” appearance of dead/ necrotic cells Granuloma= collection of lymphocytes/ inflammatory cells
Explain why smokers are most likely to get chronic bronchitis.
Smoking—> inhale a bunch of junk/ carcinogens—> respiratory system responds by increasing the number of mucinous glands in the walls of the bronchi to produce more mucous to deal with the junk (now >50% of the wall is made of mucinous glands rather than the normal <40%, by the Reid index)—> cough up cups or buckets of mucous. (Chronic bronchitis is characterized by hypertrophy of the bronchial mucinous glands and defined by cough lasting 3+ months over 2+ years).
Why do you have increased risk for infection and cor pulmonale in chronic bronchitis?
You have mucous plugs (plugs up bronchi airways) and any time you have a blocked tube you increase risk for infection (bacteria/ organism can’t escape and you have impaired defenses against them).
You get widespread vasoconstriction (inc BP, dec blood flow) in the lungs bc poorly ventilated areas try to shunt blood over to another area of the lung. Problem is all the areas are poorly ventilated from the mucus plugs/ obstruction impairing gas exchange so you get vasoconstriction all over—> inc BP that the right heart has to pump against—> right sided HF (called “cor pulmonale” when right sided HF is due to pulmonary cause).
Hypoxia (low oxygen)/ poor ventilation will cause vasodilation systemically (to inc blood flow). But, in the lungs this condition will cause vasoconstriction (to dec blood flow/ shunt the blood over to an area of the lungs that will be able to do better gas exchange with the blood). Explain how this problem is different in lobar pneumonia vs in chronic bronchitis.
Lobar pneumonia—> inflammation is just in one lobe of the lung—> that area vasoconstricts to shunt blood over to a healthier area of the lung so the blood will get good gas exchange (get rid of CO2 waste and get a hold of more oxygen to deliver to organs in the body). This is a good thing.
Chronic bronchitis—> you’ve got a problem all over (excessive mucus plugging up the bronchi all over the lungs and blocking/ impairing gas exchange so that it’s not as effective)—> widespread vasodilation all over the lungs (every part of the lung is trying to shunt the blood to another healthier area…but there is no other healthier area…). This is bad. Can lead to right sided HF/ cor pulmonale since the heart has lots more pressure to pump against (vasoconstriction inc BP).
What is the simple definition of emphysema?
Destruction of alveolar air sacs due to imbalance of protease and anti-proteases.
What are the 2 ways you can get emphysema?
1) smoking (most common!!)—> too many proteases
2) A1AT (alpha-1 antitrypsin) deficiency—> not enough anti-proteases
Explain the balance in proteases and anti-proteases that normally exists and how that balance is destroyed in emphysema.
Defense at the bottom of the lungs= alveolar macrophages. They eat the minimal debris that gets down to the bottom of the lungs—> inflammation—> release of proteases (enzymes that eat proteins, byproduct of inflammation). To protect against too much inflammation/ damage by proteases, our bodies make anti-proteases. They are normally balanced (proteases= anti-proteases).
Emphysema from smoking—> lots of inflammation going on to deal with all the chemicals you inhaled into your lungs—> lots of proteases! Your body can’t make enough anti-proteases to deal with the damage. (Proteases»_space; anti-proteases).
Emphysema fro A1AT deficiency—> inability to get the anti-proteases made in the liver out into the blood to do their job (anti-proteases < proteases).
What is the main anti-protease that neutralizes proteases called?
Alpha-1 anti-trypsin (A1AT)
Explain the pathophysiology of emphysema due to smoking. Also explain why these patients will breathe with pursed lips (“pink puffers”).
Smoking—> lots of inflammation going on to deal with all the chemicals you inhaled into your lungs—> lots of proteases! Your body can’t make enough anti-proteases to deal with the damage. (Proteases»_space; anti-proteases). The proteases damage the alveolar walls—> loss of elasticity (alveoli become like “grocery bags” instead of “balloons”). This is a big problem in the bronchioles bc there is no cartilage there to keep these airways open. Instead, they rely on the surrounding alveolar sacs to keep the walls open. Since the walls of the surrounding alveoli are destroyed, the walls of the bronchioles will be dragged in/ collapse when air goes out during exhalation (they have a problem getting air out= obstructive). By breathing slowly with pursed lips, they create a back pressure that helps keep the bronchiolar walls open and helps air get out.
*The emphysema is centriacinar (affects the airways in the center of the lungs where smoking irritants deposit) and affects upper lobes (smoke rises).
Explain the pathophysiology of emphysema due to A1AT (alpha-1 antitrypsin) deficiency. Also explain why these patients will breathe with pursed lips (“pink puffers”).
A1AT deficiency—> inability to get the anti-proteases made in the liver out into the blood to do their job (anti-proteases < proteases). You might get liver cirrhosis (the deficiency is due to a misfolded mutated protein—> mutant A1AT builds up in the ER of liver cells—> liver damage). The proteases damage the alveolar walls—> loss of elasticity (alveoli become like “grocery bags” instead of “balloons”). This is a big problem in the bronchioles bc there is no cartilage there to keep these airways open. Instead, they rely on the surrounding alveolar sacs to keep the walls open. Since the walls of the surrounding alveoli are destroyed, the walls of the bronchioles will be dragged in/ collapse when air goes out during exhalation (they have a problem getting air out= obstructive). By breathing slowly with pursed lips, they create a back pressure that helps keep the bronchiolar walls open and helps air get out.
*The emphysema is panacinar (affects airways all over) and affects lower lobes (remember it’s the opposite of that from smoking).
Panacinar emphysema. What is the etiology?
A1AT (alpha-1 antitrypsin) deficiency. (If it were due to smoking, it would be centriacinar)
Lung pathologies tend to be centriacinar/ affect the middle part of the lung in smokers. Why?
Think about really basic anatomy. You smoke and those chemicals first contact the center tubes (bronchi, bronchioles) of the lung. In contrast, lung cancers that typically affect non-smokers are often seen in the periphery of the lungs.
Regarding A1AT (alpha-1 antitrypsin) deficiency, what’s the clinical difference between heterozygotes PiMZ and homozygous PiZZ?
M= normal allele. Z= mutated allele. Heterozygotes PiMZ (one good allele, one bad allele) have less anti-trypsin working to combat the inflammation damage of the proteases but these people are generally asymptomatic. Unless they take up smoking then they are at extra high risk for emphysema! Homozygotes PiZZ (2 bad alleles) likely have panacinar emphysema and liver cirrhosis (they’ve got the disease). *remember “PiZZ is the bad one just like PiZZa is bad for you”
Why do emphysema patients get weight loss and barrel-chest?
They have to work so hard to breathe/ get air out that they spend a lot of energy/ burn calories just breathing—> weight loss.
Alveolar sacs are destroyed (lost elasticity) in this disease so the chest wall will win the “tug of war”(where forces from the lungs push in and chest wall pushes out)—> chest pushes out—> “barrel-chest”
Why do emphysema patient gets hypoxemia?
Proteases > anti-proteases —> destruction of alveoli (loss of elasticity)—> destroyed alveoli= destroyed capillaries since they are intertwined (can also think of it as destroyed alveoli= impaired gas exchange)
Why is cor pulmonale a complication of emphysema?
In emphysema you have poor oxygenation going on (mostly in center, upper lobes with smoking and lower lobes with A1AT deficiency, but if severe enough it’s kinda all over)—> vessels in the lung vasoconstrict to shunt blood away from poorly ventilated area…but the problem is vessels all over the lung are clamping down, trying to send blood to a better place to get oxygenated, but there is no better place. Widespread vasoconstriction in the lungs increases the BP the right heart has to pump against—> cor pulmonale (right HF due to pulmonary cause).
Define asthma.
Reversible airway bronchoconstriction due to a stimuli (usually an allergic stimuli).
(*note: bronchoconstriction will happen where there is smooth muscle, so from the trachea down to the respiratory bronchioles in the respiratory tree.)
A patient presents with breathing problems and liver problems. Their condition is due to misfolding of a mutated protein. What are you thinking?
Emphysema due to A1AT (alpha-1 antitrypsin) deficiency
A1AT= anti-protease. In this condition, mutated A1AT accumulates in the liver (where it is made) and is unable to go out into the bloodstream so it can defend against proteases causing damage when there is inflammation in the lungs. They get liver cirrhosis from the build up of this protein in the liver and emphysema—> breathing problems due to the imbalance of proteases»_space; anti-proteases—> destruction of alveolar air sacs (loss of elasticity to keep the bronchiole walls open when air is released).
Asthma involves what type of hypersensitivity reaction? What are the 3 main cytokines released by Th2 cells and what is the role of each of these cytokines?
Type I hypersensitivity (allergies). Th2 cells release IL-4, 5, and 10.
IL-4–> mediates class switch to IgE
IL-5–> attracts eosinophils
IL-10–> stimulates Th2 cells, inhibits Th1 cells
(*kind of like an anaphylactic allergic reaction, such as from a peanut allergy, but instead of systemic, in the case of asthma the allergen/ trigger causes a response just in the respiratory tract/ airways)
When does asthma usually present?
In childhood
Describe the inflammatory process that goes on during an asthma attack.
Re-exposure to allergen—> IgE-mediated degranulation of mast cells—> release of Histamine and generation of leukotrienes (C4, D4, E4 from the arachadonic acid pathway) leading to bronchoconstriction and inflammation.
10 year-old boy presents with dyspnea, wheezing, productive cough with spiral-shaped mucous plugs (Curschmann spirals) and eosinophil-derived crystals (Charcot-Leyden crystals). Diagnosis?
Asthma.
Asthma can arise from non-allergic causes (“non-atopic asthma”) such as what? (4 things)
1) exercise
2) viral infection
3) aspirin (“aspirin-intolerant asthma”)
4) occupational exposure
What is bronchiectasis?
Permanent dilation of bronchioles and bronchi—> loss of airway tone (air trapping). You can’t get air out appropriately (it’s obstructive) kind of like how you feel air coming out the other end of a straw you blow into, but wouldn’t feel air coming out if you were blowing into a huge pipe wider in diameter than your head. This abnormal dilation of the airways is a result of inflammation—> necrosis from CF, Kartagener syndrome, a tumor, necrotizing infection, or allergic bronchopulmonary aspiragillosis.
A cystic fibrosis patient presents with dyspnea, cough, and foul-smelling sputum. What obstructive pulmonary disorder may explain the patient’s symptoms?
Bronchiectasis (permanent dilation of the bronchi and bronchioles from inflammation—> necrosis to airway walls. This loss of airway tone—> air trapping/ hard to get air out). Note: sputum is foul-smelling bc there is mucus plugging and it stays there for a while before exiting by a cough.
What is Kartagener syndrome? What obstructive pulmonary disorder is it associated with? What are 3 other medical conditions it’s associated with?
Bronchiectasis (Kartagener syndrome= inherited defect of the Dynein arm of cilia—> lack of cilia to pump mucous out of lung—> inc infection and inflammation—> damage to airways—> permanent dilation of the bronchi and bronchioles. This loss of airway tone—> air trapping/ hard to get air out). The other 3: sinusitis (messed up mucociliary defense system to push gunk out—> inc risk of infection), infertility (poor motility of sperm), and situs inversus (position of major organs is reversed, for ex: heart is on right side of chest).
Kartagener syndrome is an inherited defect of what specific component of cilia?
The dynein arm
An inherited defect of the dynein arm necessary for ciliary movement is called what?
Kartagener syndrome
What are “interstitial diseases of the lung?”
When you have fibrosis in the intersitium of the lung. This affects gas exchange and makes it difficult to fill the lungs with air (restrictive pulmonary disease).
In idiopathic pulmonary fibrosis, what factor from injured pneumocytes induces fibrosis?
TGF-beta
The late-stage of what restrictive pulmonary disease includes diffuse fibrosis and “honeycombing” of the lungs?
Idiopathic pulmonary fibrosis
What is Pneumoconioses?
Interstitial fibrosis due to occupational exposure (alveolar macrophages engulf foreign particles and induce fibrosis).
Shipyard worker with breathing problems. What are you thinking?
Asbestosis (pneumoconioses, or restrictive lung disease due to occupational exposure in this case of asbestos. Alveolar macrophages engulf the particles—> fibrosis).
Sand blaster with fibrotic nodules in the upper lung. Diagnosis?
Silicosis. (Type of pneumoconioses, or restrictive lung disease due to occupational exposure, in this case of silica. Alveolar macrophages engulf the particles—> fibrosis).
Coal miner with black lung and rheumatoid arthritis. What’s a likely diagnosis?
Coal workers’ pneumoconioses (restrictive lung disease due to occupational exposure of carbon dust. Alveolar macrophages engulf the particles—> fibrosis).
NASA/ aerospace worker presents with noncaseating granulomas. What are you thinking?
Berylliosis (type of pneumoconioses, or restrictive lung disease due to occupational exposure, in this case of Beryllium. Alveolar macrophages engulf the particles—> fibrosis).
Which pneumoconioses (restrictive lung disease due to occupational exposure) presents like sarcoidosis? How is it similar to sarcoidosis and how can you tell it apart?
Berylliosis. Similar in that it has noncaseating granulomas in lung, hilarity lymph nodes, and systemic organs. The path looks the same but the pathophys is driven by Beryllium exposure. The give away that the question is talking about Berylliosis (not sarcoidosis) is a Beryllium miner or person who works in the aerospace industry (like NASA).
What pneumoconioses (restrictive lung disease caused by occupational exposure) increases risk for TB?
Silicosis (seen in sand blasters and silica miners, the silica inhibits phagolysosome formation within macrophages and leads to fibrotic nodules in the upper lobes of the lungs)
Why does sarcoidosis cause hypercalcemia?
“1-alpha hydroxylase activity of epithelioid hisiocytes converts vitamin D to its active form” (basically, the granulomas can activate vitamin D—> inc calcium absorption)
A sputum sample is taken from an asthma patient and evaluated by a pathologist. The histo slide shows Charcot-Leyden crystals. What are these crystals made of?
Eosinophils
What are causes of primary and secondary pulmonary HTN?
PRIMARY: BMPR2 mutation (gene that inhibits smooth muscle proliferation)—> proliferation of vascular smooth muscle—> higher pressure developed in pulmonary vasculature
SECONDARY: due to hypoxemia (COPD, interstitial lung disease) or inc volume to pulmonary circuit (CHF), can also get it from recurrent PE (pulmonary embolisms)
What is the defining criteria for pulmonary HTN?
Pressure in the pulmonary circuit >25 (normal = 10)
Steeple sign and thumprint sign on x-ray. What is it?
Croup (most likely caused by Paraflu)
In general, what causes headaches/ migraine?
Blood flow changes to the brain. (Some vasodilator drugs can cause headaches as a side effect, but vasoconstriction may also be involved in triggering headaches.)
Therapeutic supplemental oxygen given in neonatal respiratory distress syndrome (NRDS) can cause problems (too much oxygen too fast is bad). What problems (3)?
“RIB”: Retinopathy of prematurity, Intraventricular hemorrhage, Bronchopulmonary dysplasia (damage to lungs from mechanical ventilation or O2 toxicity)
What is a normal lecithin-sphingomyelin ratio? Abnormal? What does it mean?
Normal= 2. <1.5 is predictive of NRDS (neonatal respiratory distress syndrome). This is a screening test for fetal lung maturity (lecithin should spike up in late pregnancy, as this is what surfactant is made of).
Why does persistently low oxygen tension inc risk for PDA (patent ductus arteriosus)?
Low oxygen= you’re not breathing right= inc risk for PDA. Why? Because the PDA closure occurs when the baby takes a breath—closure requires oxygen (and normal breathing).
What is the minute ventilation equation? What’s the conceptual meaning?
V(e)= V(t)*RR (minute ventilation= tidal volume * respiratory rate)
Total volume of gas entering the lungs per minute.
What is the alveolar ventilation equation? What is its conceptual meaning?
Va= (Vt- Vd)* RR (alveolar ventilation= (tidal volume of 500 - physio dead space of 150) * respiratory rate)
Volume of gas per unit time that reaches alveoli
What respiratory changes do we see in the elderly…what happens to: (1) lung compliance, (2) chest wall compliance, (3) RV, (4) FVC and FVC1, (5) TLC, (6) ventilation/ perfusion, (7) A-a gradient, (8) respiratory muscle strength?
(1) lung compliance goes up (loss of elastic recoil—> more stretchy lungs)
(2) chest wall compliance goes down (inc chest wall stiffness)
(3) RV goes up (more air stuck/ left behind in lungs that you can’t get out)
(4) FVC and FVC1 go down (more air stuck/ left behind in lungs)
(5) TLC stays normal
(6) ventilation/ perfusion mismatch (kind of like emphysema to a lesser degree…more stretchy lungs and alveoli not working as well to do gas exchange)
(7) you get a HIGH A-a gradient (not as good of gas exchange)
(8) respiratory muscle strength goes down
In high altitude, do you have vasoconstriction going on in the lungs (with the purpose of shunting blood over to better ventilated areas)?
Yes. This doesn’t just occur in pathological situations like pneumonia or COPD—vasoconstriction in the lungs occurs anytime there is poor perfusion going on in the lungs).
What are examples of perfusion limited gases (3 of them)?
Oxygen (in normal health), CO2, and N2O.
*perfusion-limited means blood is the “slow guy” limiting the rate at which gas exchange can happen. So, oxygen (in normal health), CO2, and N2O get across the alveoli before the blood flows by to pick it up.
What are examples of diffusion limited gases (2 of them)?
Oxygen (specifically in emphysema, fibrosis, or exercise) and CO (carbon monoxide).
*diffusion-limited means the gas is the “slow guy” limiting the rate at which gas exchange can happen. So, blood flows by before oxygen (in emphysema, fibrosis, and exercise) and CO are able to diffuse across the alveoli to deliver that gas to the blood.
What is the Law of LaPlace (collapsing pressure equation) related to surfactant?
Collapsing pressure (P)= 2(surface tension)/ radius
So, smaller alveoli (smaller radius)= bigger collapsing pressure (alveoli are more likely to collapse). The alveoli get smaller during expiration when air is pushed out, meaning during expiration the alveoli have inc chance of collapsing. This is bad. How does the body offset this? Surfactant, which dec surface tension= dec collapsing pressure so that during expiration, the alveoli actually don’t have an inc chance of collapsing!
What’s the purpose of surfactant?
To prevent alveolar collapse (atelectasis) by decreasing surface tension.
*collapse is bad for gas exchange bc that would require inc energy to fully re-inflate alveoli with each breath
What types of diuretics (categories) are most responsible for causing K+ and H+ wasting?
Loop and Thiazide diuretics
Tare strong diuretics so a lot of Na+ is blocked from being reabsorbed—> inc delivery of Na+ to the collecting duct (CD)—> stimulates aldosterone to reabsorb more Na+ (though the CD is just for fine-tuning so not a lot gets reabsorbed and the diuretic will do it’s job of inc Na+ excretion/ inc urine)—> aldosterone reabsorbs more Na+ (pushes it to blood), but also excretes more K+ and H+ (pushes it to the urine).
What are Betamethasone and Dexamethasone?
Corticosteroids
What do we give to pregnant women at risk of premature delivery in order to prevent their baby from having NRDS (neonatal respiratory distress syndrome)?
Give Betamethasone or Dexamethasome= corticosteroids. Why? NRDS is surfactant deficiency. Corticosteroids help type II pneumocytes mature faster—> inc surfactant production—> prevent NRDS.
What does dysphagia mean?
Difficulty swallowing
Is recent travel a risk factor for epiglottitis?
No (risk factor is not getting vaccinated)
What cells can regenerate ciliated cells in the bronchioles? What cells can regenerate cells in the alveoli? (Asking what stem cells come to the rescue and heal when there’s damage)
Club cells are nonciliated but can regenerate ciliated cells in the bronchioles.
Type II pneumocytes can regenerate cells in the alveoli. They produce surfactant and act as stem cells for the alveoli (they can regenerate type I pneumocytes, which make up 95% of alveolar cells).
What are 3 big differential diagnosis to consider in a patient presenting with lower extremity edema?
- CHF (pumping problem—> heart not pumping enough blood to body so RAAS activates thinking it needs to inc BP and excess fluid backs up into venous system)
- Nephrotic syndrome (low oncotic pressure bc peeing out protein—> edema)
- Cirrhosis (the liver makes albumin, so damage to liver= damage to albumin= low oncotic pressure—> edema)
What are examples of when you hear coarse crackles on lung auscultation? Fine crackles?
Coarse crackles: pulmonary edema, COPD, CHF
Fine crackles: interstitial lung disease or pulmonary fibrosis
Why can’t you give a COPD patient 100% oxygen/ too much oxygen (if their O2 sat is 88%, you might give enough oxygen to get it up to about 93% but not all the way to 100%)?
Normally, CO2 dictates breathing, but in a COPD patient that has had constantly high CO2 levels (since gas exchange is impaired—they live in state of respiratory acidosis), oxygen takes over regulating breathing. If we give them 100% oxygen, the respiratory drive thinks they have plenty of oxygen and shuts off breathing and patient can die.
Increased tactile fremitus means what?
There is consolidation in the lungs (narrows the differential diagnosis to pneumonia, pulmonary edema, etc.)
If dull to percussion what does that mean? If percussion sounds are hyperresonant, what does that mean?
Dull to percussion= fluid (or something) in the lungs—> pleural effusion, atelectasis, or consolidation.
Hyperresonant perfusion sounds—> pneumothorax!! (Simple or tension)
What’s the difference between a simple and tension pneumothorax?
Simple pneumothorax happens on its own. Tension pneumothorax happens due to trauma. (Think T in Tension for Trauma.)
“Hyperresonant percussion sounds”
Pneumothorax!! (Either simple or tension)
Explain the tracheal deviation in pleural effusion, atelectasis, and tension pneumothorax.
Pleural effusion (fluid collected in the pleural cavity)—> trachea shifts AWAY from side of lesion (the build up of fluid shifts everything over)
Atelectasis (collapsed alveoli/ airways)—> trachea shifts TOWARD side of lesion (the compression creates a vacuum in that area and draws the trachea toward it)
Tension Pneumothorax—> trachea shifts AWAY from side of lesion (like in a car accident where you fracture a rib and it punctures the lungs—> air from the outside will get into puncture hole but air cannot escape—> air collapses the lung and there’s so much air built up that it pushes the trachea away)
*note: if the problem isn’t big enough, you may see no tracheal deviation at all.
Thick bronchial walls, lymphocytic infiltrate, mucous gland enlargement, and patchy squamous metaplasia of bronchial mucosa are all characteristics of what lung pathology?
Chronic bronchitis (most likely due to smoking).
*metaplasia= conversion of cell type (simple cuboidal/ columnar—> simple squamous)
Why would we check an amniotic fluid sample for phospholipid content?
To test for fetal lung maturity (L/S ratio= 2 is normal. <2 is suggestive of neonatal respiratory distress syndrome (NRDS), or lack of surfactant).
An organism from the lungs is stained with carbolfuchsin staining and then washes with acid (HCl) alcohol and fails to decolonize (stays carbolfuchsin/ pink). What organism could we be talking about?
This describes acid-fast staining. Must be either Mycobacterium (TB or Leprosy) or Nocardia.
A smoker who is coughing up sputum and is who has a low FEV1/FEV ratio and expiratory wheezing is most likely to have what?
COPD.
The low FEV1/FEV ratio and expiratory wheezing indicates difficulty getting air out= obstructive disease. So you think: emphysema, asthma, or bronchiectasis. Since the patient smokes, emphysema is most likely+ the productive cough with mucus indicates chronic bronchitis, so the 2 together= COPD.
How does Omalizaumab (monoclonal antibody that targets IgE) help reduce asthma symptoms? When would you give it?
Omalizaumab is a monoclonal antibody that targets IgE—> prevents IgE from binding to mast cells and causing degranulation/ release of Histamine and other inflammatory mediators—> reduces inflammation in airways.
You give this as a last resort drug (it’s expensive, very specific treatment) for severe asthmatics if inhaled corticosteroids and bronchodilators are not enough to control their symptoms.
True or false: blood flow in pulmonary circulation matches blood flow in the systemic circulation?
True. Blood is a continuous circuit and must be about even in the lungs and systemically. (If you had low blood flow to the lungs, the LV wouldn’t be getting enough blood to pump out to the body, and if you had high blood flow to the lungs, the LV would build up with too high of blood pressure to push out to the body).
What causes SVC syndrome? How does it present?
Any tumor/ mass/ thrombosis from indwelling catheters that squeezes on the superior vena cava can cause SVC syndrome. Because drainage is impaired from the top, you get swelling of the face and arms bilaterally. You also see elevated JVD and blanching with fingertip pressure. Can raise intercranial pressure—> headache, dizziness, inc risk of aneurysm/ rupture of intracranial arteries.
A patient has a lung abscess in the right lower lobe. How did the patient probably get this? What symptoms might the patient present with? Thinking of immunology, what drives formation of a lung abscess?
You get a lung abscess from aspiration of anaerobic bacteria (like Klebsiella) or from untreated pneumonia.
Symptoms: fever, cough,
What is the general mechanism of the asthma drugs cromolyn and nedocromil?
They block mast cell degranulation (“mast cell stabilizers”). By preventing release of inflammatory mediators from mast cells, they prevent bronchospasm (not for acute bronchodilation).
Does obstructive lung disease increase or decrease Functional Residual Capacity (FRC)? How about compliance?
Obstructive lung diseases= hard to get air out, so INCREASES FRC (volume of air in the lungs after breathing out normal, or RV+ ERV) and INCREASES LUNG COMPLIANCE (lungs are more stretchy/ dispensable—think of COPD where airways collapse when you breathe out, so chest pulling out wins “tug of war” vs lungs pulling in and you get a barrel chest)
A patient who recently had an MI uses 3 pillows to sleep at night so he can breathe. How does his condition affect the compliance of his lungs (increase or decrease)?
He has left-sided HF (—> backing up of fluid into lungs—> pulmonary edema). HF will DECREASE COMPLIANCE of his lungs (will make the lungs more stiff/ hard to get air in/out due to the back up of fluid).
What is the most common mutation responsible for CF (cystic fibrosis)?
Deletion of Phe508 (Phe= phenylalanine, also written as delta-F508)—a CFTR gene on chromosome 7.
This mutation is due to abnormal post-translational processing of the transmembrane protein—> results in messed up/ misfolded CFTR channel stuck in rough ER and unable to insert in cell membrane to pump Cl- across.
How can we diagnose CF (cystic fibrosis)?
Cl- sweat test. Inc [Cl-] in sweat (>60mEq/L) is diagnostic. Can confirm with genetic testing.
Can do immunoreactive trypsinogen (precursor to pancreatic enzyme high in CF patients) in newborns (take heel blood sample) to screen.
What 2 bacteria commonly cause recurrent pulmonary infections in CF patients?
Staph Aureus (gram +) and Psuedomonas (gram -)
Nasal polyps in a little kid. What should you screen for?
Cystic fibrosis
What is the inheritance pattern of CF (cystic fibrosis)?
Autosomal recessive
Patient is an alcoholic, has some sort of lesion in the right lobe of the lung, and is coughing up yellow sputum. What’s probably going on?
Aspiration pneumonia.
Alcoholics are at-risk for aspiration (vomit and then breathe it up) and aspirated stuff goes to right bronchus because there’s less curvature—> right lungs. Aspiration pneumonia is associated with lung abscess and coughing up yellow, foul-smelling sputum.
Peptostreptococcus, Prevotella, Bacterioides, and Fusobacterium belong to which class of pneumonia organisms?
Aspiration pneumonia (these are all anaerobic oral flora bacteria that can be aspirated—> pneumonia, lung abscess, cough up yellow foul-smelling sputum).
Explain how alcoholics, drug addicts, people with seizure disorders, people who had a stroke, and dementia patients are at inc risk for aspiration pneumonia.
Alcoholics and drug addicts vomit and and they are drunk or high and breathe it up so bacteria gets into lungs. People with seizures, stroke or dementia are out of it/ unconscious at a point so can also breathe up stuff they shouldn’t like vomit. Typically anaerobic bacteria that live in mouth flora—> breathe up into lungs—> aspiration pneumonia with lung abscess and coughing up sputum.
What cells secrete proteases, which plays a major role in the pathophysiology of COPD?
Macrophages and neutrophils
How does a tension pneumothorax lead to decreased cardiac output by the heart?
Air accumulates in pleural space (because outside air comes in through puncture wound, but cannot escape)—> increased pressure in chest cavity—> dec systemic venous return to the heart—> dec CO (cardiac output)
“Rust colored sputum” along with cough, fever…what is it most likely?
Strep pneumo! (Rust colored sputum + typical pneumonia symptoms= strep pneumo)
**plus, strep pneumo is the most common community-acquired pneumonia, so it’s always a good guess if you have to guess
What are the 5 things to diagnose pneumonia?
- Productive cough w/ sputum
- Fever (*could have low temp if really sick)
- Increased oxygen demand/ SOB
- Leukocytosis (high WBC count suggestive of an infection)
- Chest x-ray suggestive on pneumonia
Pneumonia secondary to measles will show what on histo?
Giant cells. Measles pneumonia—> can turn into giant cell pneumonia.
Patient is a smoker and has a mass in their lung and has a high urine osmolarity, low serum osmolarity. What is the most likely diagnosis?
Small cell carcinoma.
Remember, this is associated with paraneoplastic syndromes (secondary disorders/ symptoms that are triggered by the cancer but seem weird and unrelated). Small cell carcinoma arises from neuroENDOCRINE cells and these cells can secrete a bunch of ADH—> SIADH (syndrome of inappropriate ADH)—> body retains lots of water so plasma concentration is low (dilute) and urine is concentrated, as in this patient.
What does the mnemonic “GRAIN” stand for to remember some findings in sarcoidosis?
G- gammaglobulinemia (Ig’s in blood) R- RA (rheumatoid arthritis) A- elevated serum ACE (bc the lungs make Angiotensin Converting Enzyme—they make more in a state of sarcoidosis) I- interstitial fibrosis N- noncaseating granulomas
What 5 things are capable of causing Bronchiectasis?
- Cystic Fibrosis
- Kartagener Syndrome (defective dynein arm of cilia)
- Tumor/ foreign body
- Necrotizing infection
- Allergic bronchopulmonary aspergillosis (from the bacteria Aspergillus, usually in asthma or CF patients)
(Bronchiectasis is permanent dilation of the bronchus and bronchioles—> loss of airway tone and air trapping, which is a obstructive lung condition where it is hard to effectively get air out)
Keratin pearls. What’s this a buzzword for?
Small cell carcinoma.
What nerve can be stimulated to help solve the problem of obstructive sleep apnea?
The hypoglossal nerve (cranial nerve 12). It causes the tongue to move forward slightly , which increases the diameter of the oropharyngeal airway so the patient can breathe better during sleep and their airway is not obstructed leading to apnea (periods w/o breathing during the night).
How can BPH affect the kidneys?
Can cause hydronephrosis (build up of pee/ pressure in the kidneys) and can even progress to acute kidney injury (AKI).
Why? Bc the prostate presses on the
What is squamous metaplasia (of the lungs) and how does it relate to the condition Barrett Esophagus?
Metaplasia= transformation of one cell type to another (reversible). In squamous metaplasia, cells within the respiratory tree (like columnar cells in the bronchus/ bronchioles or cuboidal cells in the terminal bronchioles) convert to the thinned-out squamous type of cells due to chronic exposure to irritants (like smoking).
This is similar to Barrett esophagus bc this is also metaplasia. In this condition, chronic acid reflux causes the esophageal cells that are normally squamous to become cuboidal to be “tougher” and be able to handle the acid.
In COPD, what happens to EPO levels?
They increase.
Any time you have tissue hypoxia (not getting enough oxygen to your tissues), the kidneys will make more EPO to stimulate the bone marrow to make more RBCs to deliver oxygen to the body tissues (though this isn’t a very helpful way of trying to compensate in COPD because those extra RBCs will have difficulty getting oxygenated—the problem lies in the lungs). This is called secondary polycythemia (inc RBCs).
Where is the most common site of metastasis?
The lung. (For example, if you have kidney cancer like Clear Cell Carcinoma, where is it most likely to spread? To the lungs.)
Diarrhea + coughing up sputum in a smoker. What bacteria is most likely responsible?
Legionella
Which lung cancer is central, associated with smoking, and positive for Chromogranin, neuron-specific endolase, and synaptophysin?
Small cell carcinoma (note that these markers are neuroendocrine markers, which makes sense bc small cell carcinoma arises from neuroendocrine cells)
Spontaneous pneumothorax (from rupture of blebs) most commonly occurs in what region of the lungs—in tall, thin guys? In COPD patients?
Tall, skinny guys—> base of the lungs (think of it as their lungs are so tall the weight of it pulls down and causes blebs at the lung bases that can rupture and release air)
COPD patients—> apex of the lungs (think smoke rises)
Patient has family history of lung and liver disease. He’s a smoker, but only has a 5 pack year history. Now he has a low FEV1/FVC ratio consistent with obstructive lung disease (COPD). What is the most likely diagnosis. Which region of the lungs is most likely affected by the disease?
COPD due to Alpha-1 antitrypsin deficiency
Lower lobes of lungs (remember the pathology affects the liver bc the anti-protease alpha-1 antitrypsin gets trapped in there in the ER of hepatocytes after being made and the lower lobes of the lungs are right on top of the liver, so the disease affects that area *also it is panacinar, meaning the entire alveoli are affected, not just the closer areas hit by the cigarette smoke)
Can giving oxygen help a PE (pulmonary embolism)?
Yes. A PE means a blood clot is blocking blood flow in the lungs. This is a V/Q mis-match. Blood gets shunted to other areas of the lungs, but the alveoli can’t keep up with oxygenating all the extra blood (so the patient will have hypoxemia, or low oxygen, but normal or even decreased CO2). However, if you push oxygen into the patient, you can improve the ventilation of this blood.
Where is surfactant released from (be specific) and what’s its function?
Released from lamellar bodies of type II pneumocytes (alveolar cells). It’s job is to dec surface tension to prevent alveolar collapse (atelectasis).
Newborn baby with ground glass appearance on X-ray and under respiratory distress. What is going on?
Neonatal Respiratory Distress Syndrome (NRDS), which is alveolar collapse (atelectasis) due to lack of surfactant
What is the Law of LaPlace equation for collapsing pressure? Mathematically, what effect does surfactant have on this equation?
Collapsing pressure= 2(surface tension)/ radius
When radius is small (alveolar are small as they are due to alveolarization in development), there’s increased collapsing pressure (alveoli have inc tendency to collapse). Surfactant decreases surface tension, so it offsets this and it decreases collapsing pressure (alveoli have dec tendency to collapse).
Pulmonary infiltrates and hilar lymphadenopathy in a young woman (accompanied by other random symptoms). What are you thinking?
Sarcoidosis
What’s the treatment for sarcoidosis?
Oral glucocorticoids (steroids) like Prednisone (though some patients don’t require treatment—depends on how severe)
A guy has community-acquired pneumonia (CAP), lobar pneumonia. He is coughing up green sputum. Why is his sputum green?
Due to myeloperoxidase. This is a blue-green pigmented molecule in neutrophils that is released and catalyzes a reaction (forms hypochlorite acid) during phagocytosis of bacteria.
What’s the most common cause of community-acquired pneumonia (CAP) in an HIV patient?
Strep pneumo! This is true for everyone, regardless of whether or not the person is HIV+. Yes, having HIV puts you at risk for many other rare types of pneumonia (and pretty much anything bc your immune system sucks), but strep pneumo is still the most common in this population.
